{"title":"The influence of megadose methylprednisolone on experimental myocardial infarct size.","authors":"C H Shatney, R C Lillehei","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Prior work in our laboratory demonstrated a significant reduction of infarct size following early or late administration of 30 mg/kg of methylprednisolone sodium succinate (MP). This study was designed to determine the influence of larger doses of MP on infarct volume. Healthy anesthetized mongrel dogs with similar cardiac anatomy underwent ligation of the distal third of the LAD coronary artery. Following ligation, animals were randomly placed into control or treatment groups. Treated dogs received an IV bolus of either 50 mg/kg MP at 15 minutes (MP-50) or 30 mg/kg MP at 15 minutes and 1 hour later (2MP-30). Animals were then monitored for 6 hours, sacrificed, and the heart removed. The left ventricle was dissected from the heart, weighed, sectioned, and incubated in nitro-blue tetrazolium solution, an LDH stain. Unstained tissue (infarct) was dissected from the slices and weighed, and infarct volume was calculated. Among 20 untreated animals the infarct size was 14.5% +/- 4.3% of the left ventricle. Treatment with 2MP-30 or MP-50 significantly reduced infarct volume to a similar degree (9.1%-9.6%). There was no difference in the effect on infarct size by \"megadose\" MP compared to previous results with one injection of 30 mg/kg MP. Therefore, the early use of MP at doses above 30 mg/kg confers no additional protection to the ischemic myocardium.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"187-93"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D E Fry, R N Garrison, R D Rink, J Casey, M M DeCamp, J D Richardson
{"title":"An experimental model of intraabdominal abscess in the rat.","authors":"D E Fry, R N Garrison, R D Rink, J Casey, M M DeCamp, J D Richardson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Suitable small animal models of intraabdominal abscess are not available. We have developed a reliable model of intraabdominal abscess in the rat by fasting the animal overnight, devascularizing and ligating the cecum, and injecting 2.5 X 10(8) Escherichia coli and 2.5 X 10(9) Bacteroides fragilis into the ligated cecum. This model results in 39% coli acute mortalities within 48 hours from acute peritonitis, and abscess in 76% of survivals. Subsequent abscesses are 1.0--1.5 ml in volume and contain 4 X 10(8) E coli/ml of pus and 1.4 X 10(9) B fragilis/ml. This model allows chronic evaluation of sepsis in small animals and provides a convenient means to study the abscess microenvironment.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Studies of the mechanism of hypoxic pulmonary vasoconstriction.","authors":"I F McMurtry, S Rounds, H S Stanbrook","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The intrapulmonary mechanism by which airway hypoxia causes pulmonary arterial constriction is poorly understood. It is generally believed that hypoxia either elicits the release of a chemical mediator from the lung parenchyma or has a direct excitatory effect on the smooth muscle of the peripheral pulmonary arteries. We are testing the working hypothesis that hypoxia acts directly on the vascular smooth muscle to depress the rate of mitochondrial oxidative phosphorylation and to cause shifts in cytoplasmic metabolite concentrations, which then lead to membrane depolarization, calcium influx, and contraction. Results from studies of isolated perfused rat lungs with pharmacologic inhibitors of oxidative phosphorylation, glycolysis, and calcium influx have provided indirect support for the hypothesis; but a simpler in vitro preparation allowing direct measurements of energy metabolism, membrane electrical activity, calcium fluxes, and muscle tone is needed. Additional experiments have shown that inhibitors of membrane K+ conductance allow hypoxic contractions of isolated vascular smooth muscle; and such a preparation might be useful as an in vitro model of hypoxic pulmonary vasoconstriction.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"21-33"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17353373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Respiratory monitoring in acute multiple organ system failure.","authors":"C A Guenter","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Respiratory failure is a common sequel to and a major cause of death in patients with multiple organ system injury. Detailed patient care requires monitoring of lung mechanical properties, gas-exchange, and oxygen transport in the blood. Furthermore, early recognition of lung edema, lung infection, or impaired respiratory muscle function may permit therapeutic maneuvers to prevent progressive deterioration of lung function. Unfortunately, each intervention carries with it a significant risk. Consequently, monitoring must include assessment of the adverse effects of oxygen, mechanical ventilation, artificial airways, and intravascular catheters. Shrewd analysis of limited data may commonly be more effective than sophisticated invasive monitoring with its attendant risks.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"209-17"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A review of the skin and muscle hemodynamics during hemorrhagic hypotension and shock.","authors":"R F Bond","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The primary objective of this study was to compare the hemodynamic responses in a vascular bed known to exhibit decompensation (ie, skeletal muscle) with a nondecompensating bed such as the cutaneous vascular bed during systemic and local reductions in perfusion pressure induced by hemorrhage and sequential inflow arterial occlusion. The secondary objective was to examine the mechanisms which may be responsible for skeletal muscle vascular decompensation. Systemic hypotension was produced by a stepwise hemorrhage of 5 ml/kg body weight with 5-minute intervals between bleedings. The carotid sinus impact was examined during bilateral carotid artery occlusion. The intrinsic effects were evaluated during reductions in local perfusion pressure. The data show that skeletal muscle vasculature exhibits autoregulation but skin vasculature does not. Both vascular beds respond to acute hemorrhage by vasoconstriction; however, the vasoconstriction in the skin occurs as a result of increased plasma levels of catecholamines acting on alpha receptors with no neural component, whereas the vasoconstriction in skeletal muscle occurs as a result of both neural and humoral hyperactivity. The data presented also suggest that the skeletal muscle vascular decompensation occurring late in shock is the result of prostaglandin inhibition of a hyperactive sympathetic nervous system.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"53-70"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Plasma fibronectin and resistance to thrombosis during sepsis.","authors":"J E Kaplan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Previous studies have suggested that plasma fibronectin is a component of the physiological antithrombotic mechanism and is related to resistance to cardiopulmonary failure during sepsis. The current study addresses the hypothesis that fibronectin deficiency results in increased sensitivity to thrombosis during sepsis, whereas increased fibronectin results in enhanced resistance. Rats were injected with purified fibronectin, antiserum to fibronectin, antiserum to albumin or vehicle prior to intraaortic infusion of saline, live Escherichia coli (10(7)--10(8)/100 gm) or E coli endotoxin (0.001--0.1 mg/100 gm). Infusion of the higher doses was associated with greater mortality in antifibronectin groups than the other groups. Mean arterial blood pressure fell transiently in all groups following injection of antifibronectin but not following the other pretreatment. Both endotoxin and bacterial infusion resulted in severe thrombocytopenia in antifibronectin-treated animals and to a lesser extent following antialbumin. Fibrinogen consumption was increased in all groups after antifibronectin treatment in bacteria infused animals after pretreatment with antialbumin or fibronectin. Fibrin degradation products were increased by bacterial infusion in animals treated with either antiserum. The current data support a relationship between plasma fibronectin and resistance to thrombosis. The relationship was not as clear-cut as that previously observed for nonseptic thrombotic states.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"159-72"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of phentolamine on insulin levels and insulin responsiveness in endotoxicosis.","authors":"J P Filkins","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"185-90"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The improvement in endotoxin-induced redistribution of organ blood flow by inhibition of thromboxane and prostaglandin synthesis.","authors":"G E Tempel, J A Cook, W C Wise, P V Halushka","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"209-18"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inhibition of endogenous thromboxane synthesis by exogenous prostacyclin during endotoxemia in conscious sheep.","authors":"J T Flynn, R H Demling","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The relationship between prostacyclin and thromboxane activity in plasma or lymph of endotoxemia sheep was studied to better understand the physiologic significance of these two vasoactive compounds. Conscious sheep received either endotoxin alone or endotoxin plus a five-hour infusion of prostacyclin. Endotoxin alone produced a pulmonary arterial hypertension, a significant decrease in cardiac output, an increase in the lung lymph flow rate, and a leukopenia. Plasma prostacyclin and thromboxane concentrations were elevated to the same extent, while pulmonary lymph thromboxane concentrations were greater than those of prostacyclin. The administration of exogenous prostacyclin significantly attenuated the hemodynamic changes following endotoxin, but not the leukopenia. During the prostacyclin infusion, plasma and lymph prostacyclin concentration were tenfold higher than those seen with endotoxin alone, while thromboxane concentrations were six to eightfold lower. Thus, high circulating prostacyclin concentrations resulted in an inhibition of thromboxane production with an associated attenuation of the hemodynamic response to endotoxin.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"199-207"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}